UPPER & LOWER MOTOR NEURON
lesion
By
Prof/Faten Zakaria
*
Ph.D
Professor of phyiology
Consultant of neurophysiology
Department of Physiology
College of Medicine, King Saud UniversityKing
Saud University
Objectives
•Appreciate what is meant by upper and lower
motor neurons
•Explain manifestations of upper and lower
motor neurons lesions
•Know effects of lesion in pyramidal tracts at
various levels
•Know effects of lesion in the internal capsule
•Explain the manifestations of complete spinal
cord transection and hemisection.
*
Cerebral Dominance : The Dominant
Hemisphere
* hemisphere giving out the pyramidal tract
usually has more influence than the other
hemisphere and is called the “ Dominant
Hemisphere “ .
* About 90 % of people are right-handed, and
consequently their Dominant Hemisphere is
on their left cerebral hemisphere .
* The remaining 10 % of people have their
right cerebral hemisphere as the Dominant
Hemisphere , and therefore they are lefthanded & their speech center in the right
hemisphere.
3
10/1/2015
*
*
Upper Motor Neuron
Lesion,UMNL
Lower Motor Neuron
Lesion,LMNL
Can be due to
Can result from
(1) Cerebral stroke by
haemorrhage , thrombosis or
embolism
(1) Anterior horn cell lesions ( e.g.
, poliomyelitis, motor neuron
disease )
(2) Spinal cord transection or
hemisection
(2) Spinal root lesions or
peripheral nerve lesion
(Brown- Sequard syndrome )
( e.g. nerve injury by trauma or
compressive lesion)
5
1 October 2015
UMNL
LMNL
1-extent of paralysis
widwspread
localized
2-site of paralysis
Opposite side to lesion
Same side of lesion
3-Tone of muscles
Spasticity ( hypertonia )
” clasp-knife spasticity
Hypotonia ” flaccid
paralysis
4- Deep reflexes
Brisk ( exaggerated) tendon jerks
Diminished or absent
5- Superficial reflexes
absent
absent
6-Planter reflex
Extensor plantar reflex , Babinski sign
( dorsiflexion of the big toe and fanning out
of the other toes ) , or just an upgoing toe .
Absent .
7-muscle waisting
No marked muscle wasting , but minor
wasting may occur due to( disuse atrophy)
Marked muscle wasting
(atrophy)
8-Clonus
Clonus present
( rhythmic oscillation on tendon stretch )
No clonus
9-Fasciculations (seen ) .
- Fibrillation potentials by EMG
.
No fasciculations
No fibrillation potential
Fasciculations may be
seen .
& Fibrillation by EMG
*
The effect of a lesion in different parts of the motor system
Lesions of pyramidal tract cause paralysis of the UMNL type below the level
of the lesion. However, the side affected and the extent of paralysis vary
according to the site of the lesion:
* 1- In area 4:
* This leads to restricted paralysis e.g. contralateral monoplegia (paralysis of
one limb because area 4 is widespread so it is rarely damaged completely.
* 2- In the corona radiata:
* This leads to contralateral monoplegia or hemiplegia, depending on the
extent of the lesion.
* 3- In the internal capsule:
* This often leads to contralateral hemiplegia because almost all fibers are
injured
*
* The effect of a lesion in different parts of the
motor system
4- In the brain stem:
This leads to contralateral hemiplegia (crossed hemiplegia
UMNL)
+ ipsilateral paralysis of the cranial nerves of the LMNL type
(due to damage of their nuclei in the brain stem), the nerves
affected differ as follows:
1-If the lesion was in the midbrain, the 3rd & 4th are affected.
2- If the lesion was in the pons, the 5th, 6th, 7th, and 8th cranial
nerves are affected.
3- If the lesion was in the medulla, the 9th, 10th, 11th & 12th
cranial nerves are affected.
* Bilateral lesion in the brain stem is rare and leads to
quadriplegia and bilateral paralysis of the cranial nerves.
*5- In the spinal cord:
* In the upper cervical region, are fatal
due to interruption of the respiratory
pathway.
A-Bilatral lesions
- In the lower cervical region, they lead
to quadriplegia.
- In the midthoracic region lead to
paraplegia.
B-Unilatral lesions
- In the cervical region, they lead to
ipsilateral hemiplegia.
- In the midthoraic lesion they lead to
ipsilateral monoplegia in the
corresponding lower limb.
- In both conditions, there is ipsilateral
paralysis (LMNL) of the muscles at the
level of the lesion due to damage of the
spinal motor neurons
*The internal capsule
The internal capsule is the only subcortical pathway through which nerve
fibers ascend to and descend from the cerebral cortex.
•It is V-shaped, consisting of anterior & posterior limb and a genu (knee).
•It is surrounded by the putamen and globus pallidus laterally and the
caudate nucleus and thalamus medially
The anterior limb:
Contains descending fibers from the cerebral cortex to red nucleus, pons to
cerebellum, thalamus, 3, 4, and 6 cranial nerves.
The genu
Contains corticobulbar tract
The posterior limb contains:
-The descending pyramidal & extrapyramidal fibers in the anterior 2/3.
-The somatosensory radiation that ascends behind the pyramidal fibers from
thalamic nuclei to cortical sensory areas.
-The optic radiation that ascends behind the somatosensory radiation from the
lateral geniculate body to visual areas in the occipital lobe.
-The auditory radiation that ascend most posteriorly from the medial geniculate
body to auditory areas in the temporal lobe.
Effects of a unilateral lesion in the posterior limb of internal capsule
Such lesion commonly called cerebral stroke is usually caused by thrombosis or
hemorrhage of lenticulo-striate artery (a branch of the middle cerebral artery).
Patients pass into an acute then chronic stage.
1--- Acute stage
- lasts a few days up to 2-3 weeks. Acute UMNL manifestations in the opposite side:
•Flaccid paralysis including the upper and lower limbs, the lower parts of the face and
half of the tongue.
•Hemianaethesia (loss of all sensations).
•Hypotonia and areflexia.
•Loss of the superficial reflexes.
•May be +ve Babinski's sign.
-N.B: The manifestations of this stage are similar to those of LMNL. However, they
can be differentiated from the LMNL by the following:
a. The extent of paralysis is much more widespread than in LMNL.
b. There is associated hemianaethesia.
c. There may be +ve Babinski's sign
d. Absence of muscle atrophy.
* 2-Chronic(permenant or spastic )stage
The main manifestations of this stage include the following:
•Contralateral hemiplgia of the UMNL type.
•N.B: Partial recovery occurs after a variable period by the effect of the ipsilateral
corticospinal tract, extrapyramidal tracts, so, the patient can stand and even walk,
but the fine skilled movements are permanently lost.
*-Permanent loss of fine sensations in the opposite side, but the crude sensations
recover gradually.
• Contralateral homonymous hemianopia (loss of vision in the two corresponding
haves of the visual fields opposite to side of lesion due to injury to optic radiation (
injury of left optic radiation causes blindness of the right halves of visual field )
interruption of signals from the temporal part of left retina and nasal part of right
retina=loss of impulses from both left haves of both retinae = loss of both right
sides of visual field)
•Diminished hearing power in both ears (by about 50 %), because of damage of
auditory radiation.
*
4-Complete transection of spinal cord:e.g. following tumor or trauma
.
•1- if the transection is in the upper cervical
region
immediate death follows, due to paralysis of
all respiratory muscles;
•2- in the lower cervical region below the 5th
cervical segment diaphragmatic respiration is
still possible, but the patient suffers complete
paralysis of all four limbs (quadriplegia).
• 3-transection lower down in the thoracic region
allows normal respiration but the patient ends
upwith paralysis of both lower limbs
(paraplegia)--
*
Stages :A/ Spinal shock ( 2-6 weeks )
B/ Recovery of reflex activity
C/ Paraplegia in extension
a/ spinal shock
- -This stage varies in duration but usually lasts a maximum of 2-6 weeks,
after which some reflex activity recovers.
Cause:-•It is due to sudden withdrawal of supraspinal facilitation on the
spinal alpha motor neurons, namely; the continual tonic discharge
transmitted along the excitatory reticulospinal, vestibulospinal and
corticospinal tracts.
the manifestation are:
•paralysis of all muscles below the lesion (quadriplegia or paraplegia) due to
cut of umn.
•complete loss of all sensation below the level of transection.
(3) loss of tendon reflexes and superficial reflexes (abdominal ,
plantar & withdrawal reflexes ) below the level of the lesion .
*
(5) the loss of muscle tone (flaccidity) and absence of any muscle
activity (muscle pump ) lead to decreased venous return
causing the lower limbs to become cold and blue in cold weather
(6) The wall of the urinary bladder becomes paralysed and urine is retained
until the pressure in the bladder overcomes the resistance offered by the
tone of the sphincters and dribbling occurs. This is known as (retention
with overflow).
(7)Loss of vasomotor tone occurs, due to interruption of fibres that connect
the vasomotor centres in the medulla oblongata with the lateral horn cells
of the spinal cord,which project sympathetic vasoconstrictor impulses to
blood vessels. vasodilatation causes a fall in blood pressure;
Managementof this stage//This aim at rapid recovery of spinal reflex
activity which can be achieved by the following:
1)Giving antibiotics to prevent infection.
2)Giving stimulants to the spinal centers.
3)Bladder catheterization to prevent urine stasis and rectal enema to
evacuate the rectum.
4)Prevention of bed sores by cleaning the skin with antiseptics and frequent
changing the patient’s position in bed.
5)Adequate nutrition
*
B/ Stage of return of reflex activity
• As the spinal shock ends , spinal reflex activity appears again this partial
recovery may be due to:- increase in degree of excitability of the spinal cord neurons below the
level of the section ,
due to :_
1-disinhibition of motoneurons as a result of absence of inhibitory impulses
from higher motor centres
-sprouting of fibres from remaining neurons
-denervation supersensitivity to excitatory neurotransmitters .
• Features of the stage of recovery of reflex
activity
• (1) Gradual rise of arterial blood pressure due to return of spinal
vasomotor activity in the lateral horn cells. But, since vasomotor control
from themedulla is absent, the blood pressure is not stable
- vasoconstrictor tone in arterioles and venules improve the circulation
through the limbs.
*
2) Return of spinal reflexes:
1- Flexor tendon reflexes& withdrawal reflexes return earlier
than extensor ones.
- Babiniski sign ( extensor plantar reflex) is one of the
earliest signs of this stage
- Flexor spastic tone causes the lower limbs to take a position of
slight flexion, a state referred to as paraplegia in flexion.
- The return of the stretch reflex (muscle tone)
(2) Recovery of visceral reflexes: return of micturition, defecation
& erection reflexes.
- However voluntary control over micturition and defecation , and
the sensation of bladder and rectal fullness are permanently lost
( automatic micturition)
(5) Mass reflex appears in this stage
• A minor painful stimulus to the skin of the lower limbs
will not only cause withdrawal of that limb but will
evoke many other reflexes through spread of
excitation (by irradiation) to many autonomic centres.
So the bladder and rectum will also empty, the skin
will sweat, the blood pressure will rise.
-Voluntary movements and sensations are permanently
lost;
-however , patients who are rehabilitated and properly
managed may enter into a more advanced stage of recovery
(Since effective regeneration never occurs in the human central nervous system,
patients with complete transection never recover fully.)
-
*
C/ Stage of extensor paraplegia
(1) During this stage the tone in extensor muscles
returns gradually to exceed that in the flexors. The
lower limbs become spastically extended.
-Extensor reflexes become exaggerated, as shown by
tendon jerks and by the appearance of clonus.
-The positive supportive reaction becomes well
developed and the patient can stand on his feet with
appropriate
support.
• (2) The flexor withdrawal reflex which appeared in
the earlier stage is associated during this stage with
the crossed extensor reflex.
Stage of failure of reflex activity:
This results from bad management during the recovery stage.
-Urinary tract infections and bed sores infection result in failure of reflex activity
and the patient dies from renal failure.
-The spinal centers below the level of the lesion are depressed once more leading
to:
1- Loss of the muscle tone and tendon jerks, then mass reflex, withdrawal reflex
and Babinski’s sign. The muscles become flaccid and body temperature falls.
2- Loss of the defecation and micturition reflexes resulting in constipation and
urine retention with overflow.
3- Hypotension due to depression of the spinal VC centers.
The third stage does not nowadays occur because of perfect nursing and the
administration of antibiotics; both lines of treatment guard against bed sores and
renal infections.
* Hemisection of the Spinal Cord
( Brown-Sequard syndrome)
*
Occurs as a result of unilateral transverse lesion or hemisection
of the spinal cord ( e.g. due to stab injury, bullet , car accident,or
tumor ). It interrupts the continuity of both ascending & descending
tracts at only one half
-The manifestations of the Brown-Sequard syndrome depend on the
level of the lesion.( Let us take an example of such injury involving the
thoracic spinal cord )
On the same side at the level of lesion
1.Paralysis of the lower motor neuron type, involving only
the muscle supplied by the efferent nerves from damaged segments.
2-Loss of all reflexes (both superficial and deep) mediated by damaged
segments.
3. Loss of all sensations in the areas supplied by the afferent fibres
that enter the spinal cord in the damaged segments
On the same side above the level of lesion -band of Cutaneou
hyperesthesia ( increased sensibility to pain, touch & temp. occurs in
ipsilateral dermatome due to irritation of the dorsal nerve roots by the
neighboring lesion
*
B/ Ipsilaterally below the level of the lesion :
1. UMNL/spastic lower limb (spasticity)
&CLONUS
2. Dorsal column sensations are lost/ Fine touch, twopoint discrimination, position and vibration sense are
lost. why?
Touch is impaired (but not lost) because the dorsal
column is transected. Yet, crude touch sensation still
persists because of its transmission by the opposite
intact ventral spinothalamic tract.
C/ Contralaterally below the level of the lesion :
Pain and temperature sensations are lost, Why ?
*